A highly significant clinical correlation exists between thrombocytopenia and central nervous system (CNS) manifestations in patients with systemic lupus erythematosus (SLE). An understanding of the mechanisms involved in this association may provide new insight into the pathogenesis of CNS lupus. As a first stage in developing these mechanisms, we will investigate the factors involved in the production of thrombocytopenia in SLE patients with and without CNS involvement. Platelet function will be assessed by the uptake and release of 3H-serotonin and by platelet aggregation induced by ADP and collagen. The influence of SLE plasma on the function of normal platelets, as well as the function of platelets obtained from patients with SLE, will be examined. Soluble factors will be characterized to determine whether they consist of immunoglobulin and whether this immunoglobulin is monomeric, i.e., antibody, or aggregated, i.e., immune complex. Positive data from this pilot study will enable us to explore the possible usefulness of the platelet as a marker for CNS involvement in SLE and as a model for neuronal dysfunction.